Effects of Gonadotropin-Releasing Hormone Receptor Blockade on Rat Testicular Gonadotropin and Lactogen Receptors, Steroidogenesis, and Responses to Human Chorionic Gonadotropin Stimulation*

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Abstract
Testicular endocrine regulation was studied in adult male rats after treatment with a potent GnRH antagonist analog [N-AC-D-p-Cl-Phe1,2, D-Trp3, D-Lys6, D-Ala10-GnRH (Ant.)] given in doses of 1 mg/kg at 0, 12, and 24 h. One group of animals also received an injection of [human chronic gonadotropin] (600 IU/kg) at 12 h, and all animals were killed at 36 h for hormone and receptor (R) measurements. Treatment with Ant. blocked greater than 95% of the pituitary and testicular GnRH-R, and decreased serum LH [luteinizing hormone] concentration by greater than 90%. Testicular lactogen-R content was decreased by 60% (P < 0.01), but there was no change in LH-R and FSH-R concentrations. Ant. decreased serum and testicular testosterone levels by 90%, and testicular capacity to produce testosterone in vitro by 50% (P < 0.01). No decrease was observed in production rates of cAMP and progesterone. hCG alone abolished testicular LH-R, decreased lactogen-R by 55% (P < 0.01), and GnRH-R by 65% (P < 0.01). Desensitization of cAMP and testosterone production, and an increase in progesterone testosterone ratio, were seen after hCG. hCG + Ant. treatment resulted in R, cAMP and steroid responses that were indistinguishable from those seen after hCG alone. Ant.-induced hypogonadotropism decreases testicular lactogen-R concentration and testosterone production. Testicular GnRH-R and lactogen-R are subject to heterologous down-regulation by hCG. Inhibition of the putative GnRH-mediated regulation of testis by Ant. Blockade of the GnRH-R does not change testicular response to hCG-treatment in vivo. Hence, the present observations still leave the physiological role of testicular GnRH-R open.